In a study published in Current Biology, a team of researchers from the Perelman School of Medicine identified a population of neurons in the hypothalamus region of the brain that keeps mice from sleeping when they normally would when they are activated. Activating these neurons also “wakes” them from ongoing exposure to inhaled anesthetics like isoflurane or sevoflurane, and even helps maintain the alert state when animals are dosed with anesthetics.
The study also supports a hypothesis long debated by neuroscientists: that the parts of the brain regulating sleep and waking are also capable of regulating the brain’s response to general anesthetics.
“Our findings add to evidence that the neural circuits regulating wakefulness may also be important for the exit from general anesthesia,” says study senior author Max Kelz, the Anesthesia Distinguished Professor at the Perelman School of Medicine.
The findings point to the possibility of future pharmaceuticals to actively speed the exit from anesthetic states and could also promote wakefulness that might be useful in neurologic diseases such as narcolepsy. In patients with the capacity to recover from minimally conscious states, therapeutics that engage strong wake-promoting systems could offer novel therapeutic strategies to coax the brain back to a state of conscious wakefulness.
This story is by Frank Otto. Read more at Penn Medicine News.
